AI Article Synopsis
- Esculin, an active compound from Cortex fraxini, shows promise in protecting against septic cardiomyopathy by improving heart function and reducing inflammation in a mouse model.
- Esculin treatment lowered inflammatory cell production and cytokine release, while also decreasing markers for oxidative stress and apoptosis, which was further supported by experiments on neonatal rat heart cells.
- The study suggests that Esculin works by targeting the TLR4 receptor, which helps mitigate the adverse effects of sepsis on heart cells.
Article Abstract
Background: Esculin, a main active ingredient from Cortex fraxini, possesses biological activities such as anti-thrombosis, anti-inflammatory, and anti-oxidation effects. However, the effects of Esculin on septic cardiomyopathy remains unclear. This study aimed to explore the protective properties and mechanisms of Esculin in countering sepsis-induced cardiac trauma and dysfunction.
Methods And Results: In lipopolysaccharide (LPS)-induced mice model, Esculin could obviously improve heart injury and function. Esculin treatment also significantly reduced the production of inflammatory and apoptotic cells, the release of inflammatory cytokines, and the expression of oxidative stress-associated and apoptosis-associated markers in hearts compared to LPS injection alone. These results were consistent with those of in vitro experiments based on neonatal rat cardiomyocytes. Database analysis and molecular docking suggested that TLR4 was targeted by Esculin, as shown by stable hydrogen bonds formed between Esculin with VAL-308, ASN-307, CYS-280, CYS-304 and ASP-281 of TLR4. Esculin reversed LPS-induced upregulation of TLR4 and phosphorylation of NF-κB p65 in cardiomyocytes. The plasmid overexpressing TLR4 abolished the protective properties of Esculin in vitro.
Conclusion: We concluded that Esculin could alleviate LPS-induced septic cardiomyopathy via binding to TLR4 to attenuate cardiomyocyte inflammation, oxidative stress and apoptosis.
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| http://dx.doi.org/10.1016/j.intimp.2024.111897 | DOI Listing |
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